Abstract
The opioid receptors mu, delta and kappa have recently been cloned. Here we show that kappa-agonists inhibit adenylyl cyclase activity in Chinese hamster ovary cells stably transfected with rat kappa-opioid receptor cDNA. Chronic exposure of the cells to kappa-agonists did not lead to significant desensitization of the capacity of the agonists to inhibit adenylyl cyclase. On the other hand, withdrawal of the agonist following the chronic treatment led to the phenomenon of supersensitivity ('overshoot') of adenylyl cyclase activity. Both the inhibition of adenylyl cyclase activity by the acute opioid treatment and the chronic agonist-induced supersensitivity are pertussis toxin sensitive, demonstrating involvement of Gi/Go proteins in both processes.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
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Adenylate Cyclase Toxin
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Adenylyl Cyclase Inhibitors*
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Animals
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Benzeneacetamides*
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CHO Cells
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Colforsin / pharmacology
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Cricetinae
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Cyclic AMP / biosynthesis
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Etorphine / pharmacology
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GTP-Binding Proteins / physiology
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Naloxone / pharmacology
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Naltrexone / analogs & derivatives
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Naltrexone / pharmacology
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Opioid Peptides / metabolism
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Opioid Peptides / pharmacology*
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Pertussis Toxin
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Pyrrolidines / metabolism
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Pyrrolidines / pharmacology*
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Receptors, Opioid, kappa / agonists*
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Receptors, Opioid, kappa / antagonists & inhibitors
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Receptors, Opioid, kappa / genetics
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Receptors, Opioid, kappa / metabolism
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Virulence Factors, Bordetella / pharmacology
Substances
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Adenylate Cyclase Toxin
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Adenylyl Cyclase Inhibitors
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Benzeneacetamides
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Opioid Peptides
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Pyrrolidines
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Receptors, Opioid, kappa
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Virulence Factors, Bordetella
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Colforsin
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Naloxone
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norbinaltorphimine
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Etorphine
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Naltrexone
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3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
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Cyclic AMP
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Pertussis Toxin
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GTP-Binding Proteins
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U 69593